This is an application for partial support of the inaugural FASEB summer conference on Ion Channel Regulation to be held June 14-19, 2003 at the Omni Resort in Tucson, AZ. Major topics to be covered include regulation of channel expression, distribution and activity by signaling mechanisms involving G protein cascades, second messengers, protein phosphorylation, cytoskeleton and signaling complex adapter proteins. Novel channel functions and signaling pathways will also be presented. Speakers will include prominent scientists, both established and emerging, who have made important discoveries in the past 18 months, some still unpublished. In addition to speaking, senior women will chair most sessions. Approximately 145 additional participants will be selected predominantly from pre-and postdoctoral trainees and young faculty, and priority will be given to those who present abstracts or have been historically underrepresented in science. A novel feature of this meeting will be the inclusion of discussion sessions for trainees to speak informally with speakers. Requested funds will be used to provide travel awards for junior investigators and to partially defray the costs of speakers' attendance. This meeting will alternate with and complement the biennial Gordon Conference on ion channels, which focuses on the biophysical properties of ion channel proteins, particularly in electrically excitable cells. Historically ion channel regulation research has been too biochemical for channel meetings, and too biophysical for signaling meetings. This conference is designed to bring together investigators from many disciplines, biochemistry, biophysics, cell and molecular biology, physiology and neuroscience. Many recent advances have occurred in ion channel regulation research, making this a timely and important conference topic in its own right. New structural families of ion channels have been identified that respond to novel signals and serve non-traditional cellular functions in development, in aging and in immune responses. Ion channel mutations have also been identified in human diseases of the nervous, endocrine, cardiac, vascular and renal and systems. It is expected that disruption of the signaling pathways that regulate channel activity will have similar deleterious consequences for human health, so successful prevention and treatment of these diseases will require a clearer understanding of the molecular mechanisms involved.